Abstract:
:Macrophages are involved in tumor growth and progression. They infiltrate into tumors and cause inflammation, which creates a microenvironment favoring tumor growth and metastasis. However, certain stimuli may induce macrophages to act as tumor terminators. Here we report that the calcineurin B subunit (CnB) synergizes with IFN-γ to make macrophages highly cytotoxic to cancer cells. Furthermore, CnB and IFN-γ act synergistically to polarize mouse tumor-associated macrophages, as well as human monocyte-derived macrophages to an M1-like phenotype. This synergy is mediated by the crosstalk between CnB-engaged integrin αM-p38 MAPK signaling and IFN-γ-initiated p38/PKC-δ/Jak2 signaling. Interestingly, the signal transducer and activator of transcription 1 (STAT1) is a key factor that orchestrates the synergy of CnB and IFN-γ, and the phosphorylation status at Ser727 and Tyr701 of STAT1 is directly regulated by CnB and IFN-γ.
journal_name
Cell Death Disjournal_title
Cell death & diseaseauthors
Su Z,Yang R,Zhang W,Xu L,Zhong Y,Yin Y,Cen J,DeWitt JP,Wei Qdoi
10.1038/cddis.2015.92subject
Has Abstractpub_date
2015-05-07 00:00:00pages
e1740issn
2041-4889pii
cddis201592journal_volume
6pub_type
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